Fig. 7
From: Neutrophil extracellular trap induced by HMGB1 exacerbates damages in the ischemic brain

Infiltration of immune cells and vessel damage in the ischemic brain were suppressed by intranasal administration of PAD inhibitor. a Cl-amidine (5 mg/kg) was administered intranasally after 3 h of MCAO and levels of CitH3 and numbers and morphology of microglia and blood vessels were examined after 1, 2, or 4 d of MCAO. b CitH3 levels in cortices of ischemic hemispheres after 1 or 2 d of MCAO were determined by immunoblotting using GAPDH as a loading control. c-f Coronal brain sections were prepared after 4 d of MCAO and stained with anti-Iba-1 (c), anti-F4/80 (d), or anti-laminin antibody (e). Numbers of Iba-1-positive (C, 250 μm × 250 μm) and F4/80-positive cells (D, 250 μm × 250 μm) in cortex (Ct) and striatum (St) were counted and presented as means±SEMs. Total vessel length (E, 500 μm × 500 μm) and vessel density are presented as means±SEMs (F). Scale bars in C represent 200 μm and those in D, E represent 100 μm. Sham, sham-operated animals (n = 9 from 3 animals); MCAO+PBS, PBS-treated MCAO control animals (n = 12 from 4 animals); MCAO+Cl-amidine, the Cl-amidine-administered MCAO animals (n = 12 from 4 animals). Ct, cortex; St, striatum; Lm, leptomeninges. **p, < 0.01 vs. MCAO+PBS controls